So cytoplasmic see more myosin VI immunopositivity seems to have prognostic potential also within Fuhrman grade II tumours but not only within poorly differentiated tumours. It has been reported that membranous beta-catenin immunoexpression is downregulated in conventional RCCs with low nuclear grades but higher in papillary and chromophobic carcinomas than conventional RCCs [25]. In our study, nuclear beta-catenin immunostaining was more frequently detected in cases with lower Fuhrman grades, but we found PF-02341066 ic50 no prognostic significance of beta-catenin immunostaining in RCCs. Furthermore, we detected

no differences in beta-catenin immunoexpression patterns between the different histological subtypes of RCCs. According to our study, nuclear E-cadherin expression is neither an independent prognostic factor in RCC-specific survival nor associated with the nuclear grade of the tumour. Nuclear E-cadherin has previously

been demonstrated to be associated with better prognosis of RCCs [15], and there has also been a reported downregulation Selleckchem BAY 73-4506 of E-cadherin expression in clear cell RCCs [26]. In our study population, we could not prove the prognostic importance of E-cadherin that had previously been shown in smaller study populations and with shorter follow-up times. In previous studies, nuclear E-cadherin expression was detected only in clear cell RCCs [15]. In our study, some nuclear positivity was also demonstrated in papillary and chromophobic carcinomas. According to our study, nuclear myosin VI is associated with beta-catenin but there is no relationship between myosin and E-cadherin in RCCs. Myosin VI is linked to E-cadherin and beta-catenin and participates in border cell migration where it stabilises

the E-cadherin-beta-catenin cell adhesion complex [7]. Myosin VI is a cytoplasmic protein and the significance of nuclear myosin VI immunostaining is unknown. Beta-catenin, however, can be detected in the nucleus in various carcinomas [27–30]. Nuclear myosin VI could be a regulating factor for beta-catenin or a co-worker. FAD The association between myosin VI and beta-catenin might also suggest that beta-catenin provides a molecular mechanism for signal transduction from the cytoplasm to the nucleus of the cell, thereby also influencing myosin VI gene expression. Beta-catenin plays a role in the Wnt (wingless type) pathway where the multiprotein destruction complex which involves APC (adenomatous polyposis coli) influences the phosphorylation and unphosphorylation of beta-catenin and has been demonstrated to lead to the transcription and expression of oncogenes such as c-myc and c-jun [16, 17]. Beta-catenin has also been reported to be capable of regulating gene expression by the direct interaction with transcription factors such as LEF-1 (lymphoid enhancer-binding factor), providing a molecular mechanism for a signal transmission from cell-adhesion components to the nucleus [16].